Abstract
Damage to DNA, the prime target of anticancer therapy, triggers programmed cellular responses. In addition to apoptosis, therapy-mediated premature senescence has been identified as another drug-responsive program that impacts the outcome of cancer therapy. Here, we discuss whether induction of senescence is a beneficial or, rather, a detrimental consequence of the therapeutic intervention.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Apoptosis
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Cell Line, Tumor
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Cellular Senescence*
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Cyclin-Dependent Kinase Inhibitor p16 / metabolism
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DNA / metabolism
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DNA Damage
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Humans
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Models, Biological
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Neoplasms / pathology*
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Neoplasms / therapy*
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Tumor Suppressor Protein p53 / metabolism
Substances
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Antineoplastic Agents
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Cyclin-Dependent Kinase Inhibitor p16
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Tumor Suppressor Protein p53
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DNA